Psychomotor disturbances in bipolar disorder are an expression of alterations in
volition, cognition, emotion and motor control. While psychomotor disturbances
remain a classic hallmark of severe mood disorders, there is limited knowledge
about its mediators and neural correlates.The general aim of this thesis was to obtain a better understanding of psychomotor
disturbances in bipolar disorder. Our specific objectives were to investigate
whether symptoms of psychomotor disturbances in bipolar depression
relate to neural activation in frontal-striatal networks that mediate motor function,
whether there is a differential activation within these frontal-striatal motor
networks between depressed patients with bipolar disorder and healthy controls,
and whether morphometric changes in the basal ganglia and thalamus are associated
with clinical variables in euthymic bipolar disorder that may predict impairments
in psychomotor function.In paper I, we validated a self rating scale with respect to established observer
rating scales. In a post-hoc analysis we found a psychomotor factor that we investigated
further with functional magnetic resonance imaging (fMRI) in paper
II and III.In paper II, we investigated motor execution in patients with bipolar depression.
We used task based fMRI to investigate whether self paced finger tapping
would reveal any differences in neural activation between groups, and whether
neural activation at different levels in the frontal-striatal motor loop is predicted
by the functional deafferentiation theory - framework used to explain slowed
movement in Parkinson’s disease. We could not confirm our hypotheses. In paper
III, we investigated different parts of the production of voluntary movement
using fMRI and a motor imagery task. We found significant between-group differences
in medial parieto-occipital regions during motor imagery and all other
tasks, and in cortical motor areas during motor execution. We also found decreased
activations in motor regions when there was an increase in psychomotor
disturbances.In paper IV, we investigated whether tests of psychomotor function were associated
with morphometric change in the basal ganglia or thalamus. We could
not confirm our hypothesis. However, we found significant between-group differences
in the shape of the right putamen in the absence of impaired psychomotor
function. Shape differences were located in regions connected to frontal executive
regions and motor areas. In paper V, we investigated morphometric differences
in a subgroup of bipolar disorder characterized by greater impairment
of psychomotor function in their euthymic phase. We also investigated clinical
variables associated with disease expressions, and the effect of antipsychotic
treatment, on morphometric change. We found that antipsychotic medication,
the number of manic episodes and duration of illness were associated with local
shape changes in the basal ganglia.In summary, we found that psychomotor disturbances may be considered
both a symptom and a sign, and that the neural signature of these appear to involve
both structural and functional alterations in brain regions of frontal-striatal
networks.